Opin vísindi
Opin vísindi er varðveislusafn vísindaefnis og doktorsritgerða í opnum aðgangi á vegum íslenskra háskóla og Landsbókasafns Íslands - Háskólabókasafns.
Opinn aðgangur að rannsóknaniðurstöðum er í samræmi við 10. gr. laga nr. 3/2003 um opinberan stuðning við vísindarannsóknir sem og kröfur innlendra og erlendra rannsóknasjóða. Markmiðið með opnum aðgangi er að niðurstöður rannsókna séu aðgengilegar sem flestum óhindrað og án endurgjalds á rafrænu formi. Vistun í varðveislusafninu er varanleg og ætlað að tryggja aðgang að vísindaefni íslenskra háskóla í opnum aðgangi um ókomna tíð. Varðveislusafnið Opin vísindi er tengt við rannsóknagáttina IRIS og rannsóknaniðurstöður í opnum aðgangi sem eru skráðar í IRIS eru um leið vistaðar og gerðar aðgengilegar til framtíðar í varðveislusafninu. Með því að safna þessu efni saman í eitt safn verður aðgangur að því einfaldur og þægilegur fyrir alla sem vilja kynna sér það og geta þannig notið þess öfluga vísindastarfs sem fram fer í háskólum landsins.
Varðveislusafnið er OpenAIRE / OpenAIREplus samhæft og samrýmist kröfum sem gerðar eru um birtingu rannsóknaniðurstaðna úr verkefnum sem styrkt eru úr evrópsku rannsóknaáætlununum FP7 og H2020.
Varðveislusafnið notar opna hugbúnaðinn DSpace.
Opinn aðgangur að rannsóknaniðurstöðum er í samræmi við 10. gr. laga nr. 3/2003 um opinberan stuðning við vísindarannsóknir sem og kröfur innlendra og erlendra rannsóknasjóða. Markmiðið með opnum aðgangi er að niðurstöður rannsókna séu aðgengilegar sem flestum óhindrað og án endurgjalds á rafrænu formi. Vistun í varðveislusafninu er varanleg og ætlað að tryggja aðgang að vísindaefni íslenskra háskóla í opnum aðgangi um ókomna tíð. Varðveislusafnið Opin vísindi er tengt við rannsóknagáttina IRIS og rannsóknaniðurstöður í opnum aðgangi sem eru skráðar í IRIS eru um leið vistaðar og gerðar aðgengilegar til framtíðar í varðveislusafninu. Með því að safna þessu efni saman í eitt safn verður aðgangur að því einfaldur og þægilegur fyrir alla sem vilja kynna sér það og geta þannig notið þess öfluga vísindastarfs sem fram fer í háskólum landsins.
Varðveislusafnið er OpenAIRE / OpenAIREplus samhæft og samrýmist kröfum sem gerðar eru um birtingu rannsóknaniðurstaðna úr verkefnum sem styrkt eru úr evrópsku rannsóknaáætlununum FP7 og H2020.
Varðveislusafnið notar opna hugbúnaðinn DSpace.
Flokkar í Opnum vísindum
Veldu flokk til að skoða.
- University of Iceland
- University of Akureyri
- Bifröst University
- Hólar University College
- Reykjavík University
- IRIS
- Agricultural University of Iceland
- National and University Library of Iceland
- Iceland University of the Arts
Nýlega bætt við
Erratum : Exome-wide association study reveals novel susceptibility genes to sporadic dilated cardiomyopathy (PLoS ONE (2017) 12: 3 (e0172995) DOI: 10.1371/journal.pone.0172995)
(2020-02-01) Esslinger, Ulrike; Garnier, Sophie; Korniat, Agathe; Proust, Carole; Kararigas, Georgios; Müller-Nurasyid, Martina; Empana, Jean Philippe; Morley, Michael P.; Perret, Claire; Stark, Klaus; Bick, Alexander G.; Prasad, Sanjay K.; Kriebel, Jennifer; Li, Jin; Tiret, Laurence; Strauch, Konstantin; O'Regan, Declan P.; Marguiles, Kenneth B.; Seidman, Jonathan G.; Boutouyrie, Pierre; Lacolley, Patrick; Jouven, Xavier; Hengstenberg, Christian; Komajda, Michel; Hakonarson, Hakon; Isnard, Richard; Arbustini, Eloisa; Grallert, Harald; Cook, Stuart A.; Seidman, Christine E.; Regitz-Zagrosek, Vera; Cappola, Thomas P.; Charron, Philippe; Cambien, François; Villard, Eric; Faculty of Medicine
Based on experiments conducted since this article's [1] publication, the authors have concluded that the protein-protein interaction results reported in Fig 4 are not reliable. In experiments done after the article was published, the authors observed signals for the negative control indicating that there was unspecific binding to the sepharose beads (S1 File). Furthermore, efforts to replicate the experiment using the transfection/co-immunoprecipitation protocol detailed in the article did not confirm the published results: a specific proteinprotein interaction was not observed in co-immunoprecipitation experiments using native neonate cardiomyocyte extracts (S2 File). Given these findings, the result and conclusion statements referring to a physical interaction between BAG3 and HSPB7 are not supported. Specifically: · The penultimate sentence of the ZBTB17-HSPB7 locus subsection of the Results: "Using GST pull-down experiment and co-immunoprecipitation we also observed that recombinant BAG3 interacts with HSPB7 (Fig 4)." · The fifth sentence of the second paragraph of the Discussion section: "In addition, our in vitro experiments demonstrate a physical interaction of BAG3 with HSPB7 (Fig 4) suggesting functional relationships between the 2 proteins that may be relevant for their genetic implication in DCM pathophysiology." · The seventh sentence of the second paragraph of the Discussion section: "The interaction signal of BAG3 Arg151 and Cys151 isoforms with HSPB7 was similar (data not shown), suggesting no direct effect of the polymorphism on HSPB7 binding." A member of PLOS ONE's Editorial Board confirmed that the main conclusions of the article stand are not substantively affected by this issue. The authors apologize for the errors in the published article. Supporting information S1 File. Results of co-immunoprecipitation experiment conducted in HEK cells, showing non-specific binding cells over-expressing BAG and HSPB7. (PPTX) S2 File. Experimental results of co-immunoprecipitations in native rat neonate cardiomyocytes. (PPTX).
Menopause-Related Estrogen Decrease and the Pathogenesis of HFpEF : JACC Review Topic of the Week
(2020-03-10) Sabbatini, Andrea Rodrigues; Kararigas, Georgios; Faculty of Medicine
Heart failure (HF) is a complex condition affecting >40 million people worldwide. It is defined by failure of the heart to pump (HF with reduced ejection fraction) or by the failure of the heart to relax, resulting in reduced filling but with preserved ejection fraction (HFpEF). HFpEF affects approximately 50% of patients with HF, most of whom are women. Given that the annual mortality ranges from 10% to 30% and as there are no treatments specifically directed for HFpEF, there is a need for better understanding of the underlying mechanisms of this condition. We put forward the hypothesis that the decline of estrogen at menopause might contribute to the pathogenesis of HFpEF and we highlight potential underlying mechanisms of estrogen action, which may attenuate the development of HFpEF. We also discuss areas in which additional research is needed to develop new approaches for prevention and treatment of HFpEF.
Editorial : New Insights into Estrogen/Estrogen Receptor Effects in the Cardiac and Skeletal Muscle
(2020-03-19) Lowe, Dawn A.; Kararigas, Georgios; Faculty of Medicine
Estrogen-related mechanisms in sex differences of hypertension and target organ damage
(2020-06-01) Sabbatini, Andrea Rodrigues; Kararigas, Georgios; Faculty of Medicine
Hypertension (HTN) is a primary risk factor for cardiovascular (CV) events, target organ damage (TOD), premature death and disability worldwide. The pathophysiology of HTN is complex and influenced by many factors including biological sex. Studies show that the prevalence of HTN is higher among adults aged 60 and over, highlighting the increase of HTN after menopause in women. Estrogen (E2) plays an important role in the development of systemic HTN and TOD, exerting several modulatory effects. The influence of E2 leads to alterations in mechanisms regulating the sympathetic nervous system, renin-angiotensin-aldosterone system, body mass, oxidative stress, endothelial function and salt sensitivity; all associated with a crucial inflammatory state and influenced by genetic factors, ultimately resulting in cardiac, vascular and renal damage in HTN. In the present article, we discuss the role of E2 in mechanisms accounting for the development of HTN and TOD in a sex-specific manner. The identification of targets with therapeutic potential would contribute to the development of more efficient treatments according to individual needs.
H3K27ac acetylome signatures reveal the epigenomic reorganization in remodeled non-failing human hearts
(2020-07-14) Pei, Jiayi; Harakalova, Magdalena; Treibel, Thomas A.; Lumbers, R. Thomas; Boukens, Bastiaan J.; Efimov, Igor R.; Van Dinter, Jip T.; González, Arantxa; López, Begoña; El Azzouzi, Hamid; Van Den Dungen, Noortje; Van Dijk, Christian G.M.; Krebber, Merle M.; Den Ruijter, Hester M.; Pasterkamp, Gerard; Duncker, Dirk J.; Nieuwenhuis, Edward E.S.; De Weger, Roel; Huibers, Manon M.; Vink, Aryan; Moore, Jason H.; Moon, James C.; Verhaar, Marianne C.; Kararigas, Georgios; Mokry, Michal; Asselbergs, Folkert W.; Cheng, Caroline; Faculty of Medicine
Background: H3K27ac histone acetylome changes contribute to the phenotypic response in heart diseases, particularly in end-stage heart failure. However, such epigenetic alterations have not been systematically investigated in remodeled non-failing human hearts. Therefore, valuable insight into cardiac dysfunction in early remodeling is lacking. This study aimed to reveal the acetylation changes of chromatin regions in response to myocardial remodeling and their correlations to transcriptional changes of neighboring genes. Results: We detected chromatin regions with differential acetylation activity (DARs; P adj. < 0.05) between remodeled non-failing patient hearts and healthy donor hearts. The acetylation level of the chromatin region correlated with its RNA polymerase II occupancy level and the mRNA expression level of its adjacent gene per sample. Annotated genes from DARs were enriched in disease-related pathways, including fibrosis and cell metabolism regulation. DARs that change in the same direction have a tendency to cluster together, suggesting the well-reorganized chromatin architecture that facilitates the interactions of regulatory domains in response to myocardial remodeling. We further show the differences between the acetylation level and the mRNA expression level of cell-type-specific markers for cardiomyocytes and 11 non-myocyte cell types. Notably, we identified transcriptome factor (TF) binding motifs that were enriched in DARs and defined TFs that were predicted to bind to these motifs. We further showed 64 genes coding for these TFs that were differentially expressed in remodeled myocardium when compared with controls. Conclusions: Our study reveals extensive novel insight on myocardial remodeling at the DNA regulatory level. Differences between the acetylation level and the transcriptional level of cell-type-specific markers suggest additional mechanism(s) between acetylome and transcriptome. By integrating these two layers of epigenetic profiles, we further provide promising TF-encoding genes that could serve as master regulators of myocardial remodeling. Combined, our findings highlight the important role of chromatin regulatory signatures in understanding disease etiology.